Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of calcitonin on gastric emptying of a radiolabelled test meal was examined in 8 male patients with active gastric ulcer. The patients ate the test meal twice, whilst during one of the examinations they were given synthetic salmon calcitonin (415 pmol i.v. bolus + continuous infusion during 90 min to reach an overall dose of 62.25 pmol.kg-1 body mass) and during the other one they received placebo--in randomized order, according to a double-blind study protocol. In every patient a pronounced delay in gastric emptying after calcitonin was observed --the emptying index, Ix: 2.33 +/- 0.22 x 10(-2) min-1 (placebo) vs 0.81 +/- 0.18 x 10(-2) min-1 (calcitonin), p less than 0.001. Calcitonin delayed and significantly lowered the postprandial gastrin release, as well as suppressed the postprandial insulin release with a secondary change in the serum glucose concentration pattern, whereas the serum calcium and phosphorus remained unaffected. The authors conclude that salmon calcitonin in a pharmacological dose elicits a strong inhibitory effect on gastric emptying in gastric ulcer patients.
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PMID:[Effect of calcitonin on gastric emptying after isotope-labeled solid meal in patients with stomach ulcer]. 209 24

In a double-blind placebo-controlled study, the effect of calcitonin on gastric emptying and on serum concentrations of gastrin, insulin, glucose, calcium and phosphorus after a mixed solid-liquid meal was examined in six patients with type I gastric ulcer. Synthetic salmon calcitonin 415 pmol i.v. was given as a bolus followed by a 90-min infusion to reach an overall dose of 62.25 pmol.kg-1. Gastric emptying of a radiolabelled meal was measured with a gamma camera. Calcitonin suppressed gastric emptying in all patients examined. The mean gastric transit time, MTT90, increased from 38.1 +/- 0.4 min after placebo to 43.1 +/- 0.6 min after calcitonin (P less than 0.001). Calcitonin significantly blunted the postprandial gastrin release: AUC0-90 10,398 +/- 2886 ng. l-1 min (placebo) and 8238 +/- 2573 ng. l-1 min (calcitonin), P less than 0.05, and abolished the postprandial insulin release--AUC0-90 2244 +/- 230 mU.l-1 min (placebo) vs. 638 +/- 198 mU.l-1 min (calcitonin), P less than 0.01. A steady increase in the serum glucose during calcitonin infusion, reaching up to 5.6 +/- 0.31 mmol.l-1 at the end of the infusion, was observed. Calcitonin did not significantly affect serum calcium or phosphorus concentrations. The authors conclude that a delayed gastric emptying is to be expected in patients undergoing calcitonin treatment.
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PMID:Effect of calcitonin on gastric emptying and on postprandial gastrin and insulin release in patients with type I gastric ulcer. 221 26

110 patients with benign gastric ulcer and concomitant joint diseases (rheumatoid arthritis, osteoarthrosis) were treated in a comparative short-term clinical trial to assess the relative efficacy of calcitonin (daily 100 MRC of salmon calcitonin intramuscularly), cimetidine (daily 1000 mg orally) and colloidal bismuth subcitrate (De-Nol-four times a day in doses of 5 ml diluted with 15 ml of water). Groups of patients were comparable according to age, sex, duration of ulcer disease, smoking habits, gastric acid secretion and mean ulcer size. The ulcer healing was controlled endoscopically after 2 and 4 weeks of the treatment. There was no significant difference in the ulcer healing rate between three groups neither after 2 weeks (calcitonin-36.7% of healed ulcers, cimetidine-37.5% and De-Nol-35.0% nor after 4 weeks respectively (76.7%, 72.5% and 77.5%). In the calcitonin group a gradual joint pain relief was observed in 84% of patients who complained arthralgia. The moderate side effects (headache, nausea, flush) were observed only in the patients treated with calcitonin (8 subjects). We suggest that calcitonin may be considered as a valid anti-ulcer drug in the peptic ulcer patients with concomitant rheumatological diseases especially with osteoporosis.
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PMID:Calcitonin versus cimetidine or De-Nol in gastric ulcer treatment. An endoscopically controlled trial. 307 78

The effects of different doses of Asu(1,7) eel-calcitonin, peripherally injected, on gastric secretion were studied in conscious Brattleboro rats, which are genetically deficient in vasopressin. Moreover, we evaluated the activity of this analogue on gastric ulcer formation by restraint stress. We found that 5 IU/kg Asu(1,7) eel-calcitonin decreased gastric secretion and inhibited the development of stress-induced ulcers in Brattleboro rats. These data suggest that vasopressin does not play a role in the gastrointestinal activity of Asu(1,7) eel-calcitonin.
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PMID:Inhibition of gastric secretion and stress-induced ulcers by intravenous Asu(1,7)eel-calcitonin independent of vasopressin. 362 98

The effects of different doses of (Asu1,7) eel-calcitonin, iv injected, on gastric secretion were studied in conscious rats with pyloric occlusion. Moreover, we evaluated the activity of this analogue on gastric ulcer formation by restraint stress. It was found that 2.5 or 5 Ul/kg (Asu1,7) eel-calcitonin decreased gastric acid secretion and inhibited the development of stress-induced ulcers in rats. In the isolated rat stomach the peptide at the concentrations of 1 nM to 1 microM did not modify acetylcholine, histamine or 5-hydroxytriptamine-induced contractions. These results suggest that this peripheral activity of (Asu1,7) eel-calcitonin does not involve a direct interference with cholinergic, histaminergic or serotonergic pathways at gastric level.
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PMID:Inhibition of restraint stress by systemic (Asu1,7) eel-calcitonin. 383 98

Many different experimental models for the induction of gastric ulcers have been reported in rats. Most of these experimental designs are often not reproducible and the interpretation of the results obtained is sometimes difficult. In the present study, three different models were found to give reliable and reproducible results, which could be repeated at any time of the year with different experimenters performing the procedure. To date, these methods are in our opinion, the best in designing gastric ulcer experiments and assessing the effect of pharmacological active substances. Two pharmacological active substances were investigated in the present study, pindolol, a beta-blocking agent with intrinsic sympathomimetic activity and salmon calcitonin, a hormone influencing calcium homeostasis in blood. Using all three different models no effect was seen after pindolol administration, while a strong inhibitory effect on the formation of gastric ulcers was observed after salmon calcitonin. Following ligation of the pylorus, the ulcer formation rate was significantly decreased from 80 to 33% with a significant fall in ulcer index from 2 to 0.42 and reduction of the ulcer areas from 6.6 to 0.58 mm2 (p less than 0.05). In addition, following phenylbutazone administration the appearance of gastric ulcers was diminished after salmon calcitonin from 1.4 to 0.43 and in ulcer area from 4.5 to 0.95 mm2 (p less than 0.01). These three ulcer models used in the present study were found to be very reliable as compared with other models reported in the literature and tested in our laboratory.
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PMID:The effect of pindolol and salmon calcitonin on experimental gastric ulcers in rats. 721 27

Basic fibroblast growth factor (bFGF) has well-established angiogenic and ulcer healing actions. bFGF has also been found to induce neural regeneration in the central nervous system. Thus, the present study was undertaken to clarify the effect of basic fibroblast growth factor on the regeneration of autonomic nerves in the granulation tissues following the induction of experimental gastric ulcer induced by acetic acid in rats. Rats were divided into control, acetic acid alone, and acetic acid plus acid-stable human recombinant basic fibroblast growth factor (CS23, 1 microgram/100 g body wt., every 12 hr for three days, or one or two weeks, through oral gastric intubation) groups. As a result, few autonomic nerves were recognized surrounding the newly formed arterioles and venules in the acetic acid alone group. In the CS23-treated group, the cholinergic, calcitonin gene-related peptide and vasoactive intestinal peptide-immunoreactive nerves were clearly recognized near the microvessels, but few adrenergic nerves were seen even after CS23 treatment. From these observations, basic fibroblast growth factor was suggested to promote the reinnervation of the newly formed microvessels.
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PMID:Effect of basic fibroblast growth factor on reinnervation of gastric microvessels. Possible relevance to ulcer recurrence. 762 67

The healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin were investigated with reference to the enzyme activity of both prolylhydroxylase and collagenase as related to histological findings. The rats were observed by endoscopy on the 3rd day after the subserosal injection of acetic acid; rats with ulcers were divided into three groups: non-treated, and cimetidine- and calcitonin-treated. The latter two groups were treated for 7 days. Prolylhydroxylase activity in active ulcers in the non-treated group was slightly higher on the 3rd day and significantly higher on the 10th day than the activity in control rats that had received subserosal injections of physiological saline solution on the respective days. In non-treated rats, the healed ulcer on the 10th day showed lower prolylhydroxylase activity than that in the active ulcer on the same day. Cimetidine did not affect prolylhydroxylase activity, but, with calcitonin, there was higher prolylhydroxylase activity in the healed than in the active ulcer, although the difference was not significant. Interstitial collagenase showed the highest activity on the 3rd day and decreased on the 10th day in non-treated rats. Collagenase activity was higher in the cimetidine-treated group, than that in the non-treated group, and numerous peroxidase-positive granulocytes were seen in the mucosa and submucosa. Calcitonin did not affect collagenase activity. The participation of both enzymes is indispensable in the healing process and the effects of anti-ulcer agents on these enzymes must be considered.
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PMID:Wound healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin, with special reference to prolylhydroxylase and collagenase enzyme activity. 764 95

1. The aim of the present study was to determine the role of 5-HT3 receptors of the gastroprotective effect of salmon calcitonin (sCT) and sCT-induced changes in gastric, hepatic, brain and brainstem glutathione (GSH) and lipid-peroxidation (LP) levels in rats subjected to cold-immobilization stress. 2. Stress exposure resulted in ulcer formation and a decrease in GSH levels of the liver, brain and brainstem and an increase in gastric and hepatic LP (P < 0.05). 3. sCT prevented stress-induced gastric ulcer development (P < 0.01) and reversed the decrease in hepatic and brain GSH levels (P < 0.05). 4. In the present study, a 5-HT3 receptor antagonist, ICS 205,930 was used. Interestingly, the effect of the blocker on GSH and LP levels of the tissues studied was similar to those of sCT. 5. ICS 205,930 dose dependently reversed the anti-ulcer effect of sCT although it did not antagonize the effect of sCT on GSH and LP levels, but it seemed to show an additive interaction for brain and brainstem GSH and gastric LP levels with sCT.
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PMID:The role of 5-HT3 receptors in the anti-ulcer effect of calcitonin. 772 Oct 34

Gastric calcitonin gene-related peptide-like immunoreactivity (CGRP-li) was decreased in the gastric corpus of rats treated with 75% or 96% ethanol but not with 50% ethanol. The extent of gastric lesions was related to the increasing concentrations of ethanol (50-96%). CGRP-li decrease was evident already at 5 min after the 96% ethanol challenge, whereas a peptide recovery resulted 10 days after, concomitant with the healing of gastric lesions. Ethanol (96%) produced a significant decrease of CGRP-li in the whole thickness of the gastric corpus but not in the mucosal layers of the same area, indicating that the muscular layer of the gastric corpus is the zone involved in this phenomenon. Pretreatment with the selective sensory neurotoxin capsaicin induced a gastric CGRP-li decrease in the corpus and forestomach. Ethanol (96%) did not further decrease gastric corpus CGRP-li in capsaicin-pretreated rats. These findings suggest that 96% ethanol induced a decrease of CGRP-li deriving from a capsaicin-sensitive pool and that CGRP may play a role in gastric ulcer pathogenesis of haemorrhagic lesions induced by concentrated ethanol.
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PMID:Gastric lesions induced by concentrated ethanol are associated with a decrease in gastric calcitonin gene-related peptide-like immunoreactivity in rats. 830 15


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